Executive functions deficits impair extinction of generalization of fear of movement‐related pain

AbstractBackgroundGeneralization of fear of movement‐related pain across novel but similar movements can lead to fear responses to movements that are actually not associated with pain. The peak‐shift effect describes a phenomenon whereby particular novel movements elicit even greater fear responses than the original pain‐provoking movement (CS+), because they represent a more extreme version of the CS+. There is great variance in the propensity to generalize as well as the speed of extinction learning when these novel movements are not followed by pain. It can be argued that this variance may be associated with executive function capacity, as individuals may be unable to intentionally inhibit fear responses. This study examined whether executive function capacity contributes to generalization and extinction of generalization as well as peak‐shift of conditioned fear of movement‐related pain and expectancy.MethodsHealthy participants performed a proprioceptive fear conditioning task. Executive function tests assessing updating, switching, and inhibition were used to predict changes in (extinction of) fear of movement‐related pain and pain expectancy generalization.ResultsLow inhibitory capacity was associated with slower extinction of generalized fear of movement‐related pain and pain expectancy. Evidence was found in favor of an area‐shift, rather than a peak‐shift effect, which implies that the peak conditioned fear response extended to, but did not shift to a novel stimulus.ConclusionsParticipants with low inhibitory capacity may have difficulties withholding fear responses, leading to a slower decrease of generalized fear over time. The findings may be relevant to inform treatments.SignificanceLow inhibitory capacity is not associated with slower generalization, but extinction of fear generalization. Fear elicited by a novel safe movement, situated outside the CS+/− continuum on the CS+ side, can be as strong as to the original stimulus predicting the pain‐onset.